The cya, crp, rho and nus gene products modulate the expression of a wide variety of bacterial and bacteriophage genes or operons. In order to understand the regulatory processes, we are studying the structure, expression and activity of these genes. We have previously shown that the protein products of the cya, crp and rho genes are autogenously regulated. We have shown by pulse labelling of RNA and by DNA-RNA hybridization, as well as by operon fusion analysis, that the autogenous regulation of rho is at the level of transcription. We have also found, by similar analysis, that cyclic AMP is a positive effector for Rho gene expression, but also acta as a "repressor" of rho mRNA translation. This opposite control of the rho gene by cyclic AMP would maintain a constant level of Rho in cell. We are currently studying the system in vitro. We have isolated mutants in the crp gene, which make the CRP protein functional in the absence of cyclic AMP. The mutations are now being sequenced. The amino acid changes in these altered CRPs would allow us to understand the molecular mechanism of gene activation by CRP. We have found that a NusA amber fragment is still functional for anti-termination, when expressed from a multi-copy plasmid. This suggests that it is the NH2-terminal portion of NusA that is important for anti-termination.